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Functional and Phenotypical Characterization of Activated T Cells from Intra‐articular Sites in Inflammatory Joint Diseases
Author(s) -
JAHN B.,
BURMESTER G. R.,
STOCK P.,
ROHWER P.,
KALDEN J. R.
Publication year - 1987
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1987.tb02312.x
Subject(s) - t cell , lymphokine , cd8 , immunology , antigen , cd3 , biology , cytotoxic t cell , receptor , synovial membrane , t lymphocyte , microbiology and biotechnology , immune system , interleukin 2 , tcirg1 , antigen presenting cell , inflammation , in vitro , biochemistry
The presence of activated T lymphocytes bearing interleukin 2 (IL‐2) receptors and HLA class II (la) antigens accompanied by impaired T cell functions such as a decreased mitogenic responsiveness are characteristic findings, especially in intra‐articular sites in chronic inflammatory joint diseases. The objective of the present study was to further characterize these in vivo activated T cells by the investigation of IL‐2 production and a possible T cell receptor modulation. IL‐2 receptors were found to tic expressed primarily in ihe CD4 + subset. The Ia + subset expressing both DR and DQ antigens showed a weaker miiogen‐induced response as compared to the la + fraction. A decreased mitogen‐induced IL‐2 production and a lower response to anti‐CD3 monoclonal antibodies was observed with synovial T lymphocytes as compared to peripheral blood T cells. The density of the CD3 molecule, known to be closely associated with the T cell receptor, was significantly lower in intra‐articular sites, while other T cell‐specific surface molecules were expressed to a similar extent in both compartments. The decreased synovial T cell mitogenesis was not restored by the addition of lymphokines (IL‐1 and IL‐2) or blood monocytes, nor by removing CD8 + T cells. These data present further evidence for a significant T cell activation in intra‐articular sites in chronic inflammatory joint diseases. The decreased expression of the CD3 glycoprotein suggests a modulation by so far unidentified antigen(s), which could also be responsible for the weak T cell response elicited by polyclonal mitogens.